Hamilton's missing link

Hamilton's famous rule was presented in 1964 in a paper called "The genetical theory of social behaviour (I and II)", Journal of Theoretical Biology 7, 1-16, 17-32. The paper contains a mathematical genetical model from which the rule supposedly follows, but it does not provide a link between the paper's central result, which states that selection dynamics take the population to a state where mean inclusive fitness is maximized, and the rule, which states that selection will lead to maximization of individual inclusive fitness. This note provides a condition under which Hamilton's rule does follow from his central result.     

FTO and obesity: the missing link

The field of vascular molecular imaging is searching for the "holy grail" of an imaging technique that will quantitatively and reliably assess vulnerable coronary plaques. Fluorescence imaging with indocyanine green specifically identifies lipid-rich plaques in rabbits and in humans and represents a promising, though invasive, approach.     

Phototaxis,chemotaxis and the missing link

Phototaxis in Archaea employs an integral membrane complex composed of a photoreceptor that is similar to the light-driven proton pump bacteriorhodopsin, and a transducer protein that is similar to the familiar eubacterial chemotaxis receptors. Recent structural studies have revealed how these proteins are assembled in the membrane, and provide a heuristic framework for future work on the mechanism of signal transduction by this important class of molecules.     

DCAFs, the missing link of the CUL4-DDB1 ubiquitin ligase

The CUL4-DDB1 ubiquitin ligase regulates cell proliferation, survival, DNA repair, and genomic integrity through targeted ubiquitination of key regulators, yet the substrate receptors that dictate the specificity of this ubiquitination machinery have been largely unknown. Recent work identified a family of DDB1 and CUL4-associated factors (DCAFs) as substrate receptors, implicating a broad spectrum of cellular processes regulated by CUL4-DDB1.     

Histone H2AX: The missing link in AIF-mediated caspase-independent programmed necrosis

Caspase-independent programmed necrosis is a highly regulated cellular demise that displays morphological and biochemical necrotic hallmarks, such as an earlier permeability of the plasma membrane and lactate dehydrogenase (LDH) leakiness. This form of programmed cell death (PCD) is regulated by AIF, a FAD-dependent oxidoreductase, which is released from the mitochondria to the nucleus where it induces chromatin condensation and DNA fragmentation. Some years ago, it has been established that the sequential activation of poly(ADP-ribose) polymerase-1 (PARP-1), calpains, and Bax regulate the mitochondrial AIF release associated to programmed necrosis. But, what happens when AIF is in the nucleus? How does this protein induce chromatinolysis and programmed necrosis? Recently, we have unraveled some of the mechanisms underlying the nuclear action of AIF in this type of caspase-independent cell death. Indeed, AIF plays a key role in programmed necrosis by its ability to organize a DNA-degrading complex with H2AX and Cyclophiline A (CypA). The AIF/H2AX link is indeed a critical event and explains the nuclear AIF apoptogenic action. In the present article, we outline the current knowledge on cell death by programmed necrosis and discuss the relevance of the AIF/H2AX/CypA DNA-degrading complex in the regulation of this original form of cell death.     

The missing link in the eukaryotic ribosome cycle

A truly groundbreaking paper by Pisarev et al. (2007), recently published in Cell, has solved a wide gap in our knowledge of eukaryotic mRNA translation, by elucidating how ribosomes are released from mRNA after the termination step.     

Mixotrophy: the missing link in consumer-resource-based ecologies

Theoretical Ecology - The classical separate treatments of competition and predation and difficulties in providing a sensible theoretical basis for mutualism attest to the inability of traditional...